I have pulse labeled lecithin in vivo with various precursors and measured lecithin specific activity changes with time in lung parenchyma, microsomes, lamellar bodies, and the alveolar wash in premature newborn, term newborn, and adult rabbits. This proposal will extend this type of kinetic analysis of lecithin to in utero animals, and to the two acidic phospholipids, phosphatidyl glycerol (PG) and phosphatidyl inositol (PI). The results will allow a comparison of lung surfactant related phospholipid metabolic differences between in utero, newborn and adult animals. The increased lecithin stability (biological half-life) and prolonged times required for lecithin appearance at the alveolar space in the newborn will be further defined, with pulse labeling of PG and PI. The differences between newborn and adult lung lecithin metabolism will be explored by following pulse labeled lecithin in "immature" lamellar body particulate forms isolated by differential and density centrifugation. The ability of the lung to convert unsaturated to disaturated lecithin by preferential incorporation of palmitic acid into the 2-position of the molecule will be defined as to fatty acid specificity, developmental stage of the animals (premature vs newborn vs adult) and subcellular localization of the reaction products following pulse labeling in vivo. A combined approach analyzing the "development" of the lamellar body, the kinetic analysis of surfactant-related phospholipids in lung fractions and in vivo the saturation of lecithin in the in utero premature, term and adult rabbit will directly attack the differences between newborn and adult animals and the stresses of premature and term birth on the ability to maintain alveolar stability.